Preeclampsia (PE) is a devastating disorder of pregnancy that affects up to 8% of pregnant women in the United States (1). The diagnosis of PE is made by the presentation of new onset hypertension, ≥140mmHg systolic blood pressure (BP) or ≥90mmHg diastolic BP, and either proteinuria or another accompanying sign/symptom, such as renal insufficiency, thrombocytopenia, hepatic dysfunction, pulmonary edema or cerebral/visual impairment (2-4). These signs can occur suddenly and without warning. PE that presents before 34 weeks of gestation is considered early-onset and carries a greater risk for perinatal morbidity/mortality than late-onset PE that occurs at or after 34 weeks of gestation (2,3). At this time there is no cure for PE and the only effective treatment is delivery of the baby and placenta. If allowed to progress to eclampsia (PE with neurologic involvement), seizures will occur and possibly death through stroke. PE also carries the risk of significant fetal and neonatal morbidity/mortality in addition to long term health risks for mother and child (5). Despite significant research efforts to accurately predict, diagnose, and treat PE, a cure eludes us. Elucidating the pathophysiological mechanisms that can cause PE will aid in our ability to accurately prevent, manage, and treat PE in order to avoid maternal and fetal losses. Intense research efforts are focused on PE and the mouse has proven to be a useful animal model for investigating molecular mechanisms that may hold the key to unraveling the mysteries of PE in women.
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